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   
 

‡ 80% disekresi oleh epitel badan silier yang


tidak berpigmen melalui proses metabolik
aktifs yang tergantung pada jumlah enzim
(carbonic anhydrase enzyme),

‡ 20% diproduksi oleh proses pasif melalui


ultrafiltrasi dan difusi
  
   
   
      

‡ Jaringan trabekular terletak di sudut bilik


mata depan yang terdiri dari :
± Membran Descemet ^ uaris Schwalbe
± Sklera ^ tonjolan sklera
± Iris ^ tonjolan iris
± Badan Siliar ^ angle recess
      

‡ The TM is devided into three portions:


± Uveal meshwork, large spaces, resistance «,
± Corneoscleral meshwork, smaller space,
± Endothelial meshwork, major proportion of
normal resistance to aqueous outflow.
‡ Obstruction of aqueous flow usually at
trabecular meshwork ^ high IOP.
      
a. Jaringan Uvea
b. Jaringan
Korneosclera
c. uaris Schwalbe
d. Kanal Schlemm
e. Saluran
pengumpul
f. Badan Siliar
g. Tonjolan Sclera
  

|liran normal cairan


aqueous :
a. Jalur trabekular
konvensional
b. Jalur Uveoskleral
c. melalui iris
  

‡ | mengisi bilik mata belakang (BMB) ^


pupil ^ bilik mata depan (BMD) ^ keluar
dari dalam mata melalui 2 cara :
± 90% melalui jalur trabekular ^ kanalis
Schlemm¶s ^ vena episklera ^ keluar mata
± 10% melalui jalur uveosklera: melewati badan
silier ^ ronga suprachoroidal ^ sistim vena
dalam badan silier
  
| mengisi BMB pupil

Jalur trabekular 90 % BMD

Kanalis Schlemm jalur uveosklera (10%)

rongga suprakoroid badan silier


Keluar mata
Melalui vena episklera sistim vena dalam badan silier
    
 


‡ Tekanan intra okular (TIO) yg tinggi


‡ Tekanan episklera yg tinggi
‡ Kekentalan |queous : eksudat, sel darah
‡ Blok Siliar, blok pupil, sinekia posterior
‡ Sudut bilik mata depan sempit/tertutup
‡ Penyempitan pori-pori jaringan trabekula
‡ Macrofag, sel lensa di jaringan trabekula
     
‡ Normal 15 - 21 mm g,
‡ TIO > 21 mm g ^ diduga glaukoma
‡ Perubahan Diurnal TIO selama 24 jam :
± TIO lebih tinggi pada pagi hari
± TIO lebih rendah pada sore & malam hari
‡ ipertensi Okular : TIO > 21 mm g tanpa
kerusakan serabut saraf
‡ ulaukona tensi normal : normal TIO, ada gejala
glaukoma
u 
K   

‡ Neuropati diskus optikus yg ditandai


dengan :
± TIO tinggi > 21 m g
± Kematian serabut saraf optik ^ kerusakan
diskus optik
± Kerusakan lapang pandang progresif
‡ Penyebab kebutaan permanen ketiga
terbanyak
  

‡ Congenital glaucoma ^ age 0 - 2 years


‡ Infantile glaucoma ^ age > 2 years
‡ Juvenile glaucoma ^ age > 15 year
‡ Secondary glaucoma: glaucoma as a
complication from other eye disease
r 
  
   K 

‡ There are two current theories:


± The indirect ischaemic theory: IOP » -- nerve
fiber death + interfering of micro circulation of
the optic disc,
± Direct mechanical theory: IOP » -- damage
retinal nerve fiber at the optic disc.
    
  

‡ |ccording to:
± Outflow impairment: open angle and angle
closure glaucoma,
± Factor contributing IOP » : primary and
secondary glaucoma,
± |ge: congenital, infantile, juvenile, adult.
r   

‡ igh IOP is not associated with any ocular


disorder
± Open angle
± |ngle closure
± Congenital (developmental)
     

‡ |queous outflow alters by ocular / non


ocular disorders ^ IOP » :
± Secondary open angle glaucoma: pretrabecular,
trabecular and post-trabecular,
± Secondary angle closure glaucoma caused by
apposition between the peripheral iris and
trabeculum,
± Pathogenesis: anterior forces / posterior forces
    

Mechanism of obstruction in
secondary glaucoma:
a. Pre-trabecular
obstruction (membrane)
b. Trabecular obstruction
(pigment granules)
c. Secondary angle closure
by pupil block
d. Secondary angle closure
without pupil block
 

‡ Two main methods of measuring IOP:


± applanation force to flatten the cornea
± indentation force to indent the cornea
‡ The main types of tonometer:
± The Schiotz tonometer uses a plunger with a
preset weight to indent the cornea. The amount
of indentation is converted into mm g by use
of Friedenwald tables.
 
‡ The main types of tonometer:
± uoldmann tonometer consists of double prism with
3.06 mm in diameter, applanation, more accurate,
± Perkins tonometer, hand held, applanation,
± The air puff tonometer, non contact, applanation, jet of
air to flatten the cornea.
± Tono-pen
± uas Tonometer
± Electrical Tonometer

    

Î Portable, simple, low cost,


Î Measure the depth of indentation of
cornea by a plunger with specific
weight,
Î 5 mm indentation represent as each
scale of Schiotz which converted into
mm g by Freidenwald table,
Î Low accuracy because it is
influenced by ocular rigidity (high
myop, DM, corneal leucoma).
  !  
  

‡ More accurate, not influenced by ocular rigidity,


‡ The foot plate of the plunger is smaller (3.06 mm),
‡ Disadvantages: cannot be applied to
± Corneal edema
± Keratitis, corneal ulcer
± Keratokonus
± igh astigmatic
  

‡ To estimate outflow facility of |,
‡ Principal: to express fluid from the eye by
continuous pressing to the eye, maximal
flows,
‡ Placing Schiotz type tonometer 2-4 minutes,
‡ Compare IOP at 0 and after 4 minutes ^
outflow facility (C),
‡ Normal C > 0.18.
r "    
‡ Water drinking test, dark room test,
midriatic test, steroid test,
‡ Positive if IOP at the end of the tests are
more than 8 mm g,
‡ Indications:
± Narrow / closed angle glaucoma
± Normal tension glaucoma
± Bias IOP
   

‡ Three main purposes of gonioscopy:


± Identification of abnormal angle structure,
± Estimating the width of the chamber angle,
± Visualization of the angle during this following
procedures: goniotomy, laser trabeculoplasty.
       
       

‡ Schwalbe¶s line as an opaque line is a


peripheral termination of Descemet
membrane,
       

‡ Trabecular meshwork has a ground glass


appearance, stretches from Schwalbe¶s line
to scleral spur.
Consists of two part:
± The anterior, nonfunctional, non pigmented
part, whitish color,
± The posterior, functional, pigmented part,
greyish-blue translucent.
       

‡ Schlemm¶s canal, slightly darker line, deep


to the posterior trabeculum,
‡ Scleral spurs, most anterior of sclera,
narrow, dense, often shiny, whitish band.
|s a landmark for laser trabeculoplasty.
       
‡ Ciliary body stands behind the scleral spur as dull
brown band. The width depends on iris insertion.
± Curve of the corner at the margin of the ciliary body
± Iris processes
‡ The angle recess dipping of the iris, it inserts into
the ciliary body.
‡ Iris processes, small extension of the anterior
surface of the iris, inserted at the level of scleral
spur.
   
  
 
       
     
 

‡ urade IV : 45 degrees angle


III : 20 - 25 degrees angle
II : 20 degrees angle ^ closed
I : 10 degrees angle ^ closed
‡ Slit angle : less than 10 degrees,
‡ urade 0 : closed angle, iridocorneal
contact.

   


   
 
‡ 1.2 million axons pass across the retina and enter
the optic disc,
‡ Fibers from the macula ^ papillomacular bundle,
straight to the optic disc, most resistant,
‡ Fibers from temporal of macula ^ an arcuate path
around the papillomacular bundle ^ supero and
inferotemporal of the optic disc, vulnerable to
glaucomatous damage.


   
 

Nerve fiber layer anatomy




   
 

Normal nerve fiber layer




   
 

Normal nerve fiber layer Diffuse nerve fiber atrophy




   
 
‡ Scleral canal, the opening of 1.2 million nerve
fiber leaves the eye, oval, vertical, 1.75 mm in
diameter,
‡ The lamina cribrosa, plate of collagenous
connective tissue, 200-400 pore, containing retinal
nerve fiber bundles,
‡ The large pores have thin connective tissue
supports, and large nerve fibers, vulnerable to
glaucomatous damage.


   
 
‡ The optic cup, pale depression in the center of the
optic cup, absent of nerve fiber,
‡ The neuroretinal rim, tissue between outer edge of
the cup and the outer margin of the disc, the color
is pink orange, uniform width, contains nerve
fibers,
‡ Nerve fibers death ^ thinning of retinal rim,
‡ igh IOP ^ posterior bowing of lamina cribrosa,
nasalisation of central retinal vessels.


   
 

‡ The cup-disc ratio: fraction of vertical and


horizontal diameter cup and diameter of the
disc, normal c/d ratio is 0.3 or less.

   

Normal disc with small cup



   

Large physiological
cups

   
‡ Progressive loss of the retinal nerve fibers ^
notching / thinning of neuroretinal rim (NRR)
‡ The cup is enlarged :
± concentrically ^ diffuse thinning of NRR
± localized expansion ^ notching of NRR
‡ Double angulation of the blood vessel ^
bayoneting sign,
‡ |rterial and vein nasalisation,

   

‡ Cup and disc ratio > 0.6,


‡ Peripapillary atrophy at temporal region,
‡ Splinter-shaped hemorrhage on the disc
margin.

   
§  # $ 
%&  
‡ Nasally 60 degrees
‡ Temporally 95 degrees
‡ Superiorly 50 degrees
‡ Inferiorly 70 degrees
‡ The blind spot is located temporally 10-20 degrees
‡ Visual field is an island of vision surrounded by
sea of darkness, the sharpest is at the top of island.
# $   

‡ Baring of the blind spot


‡ Localized paracentral scotoma at 10 - 20
degrees of fixation at superior and inferior
quadrant ^ extension to the blind spot ^
Byerrum scotoma ^ ring scotoma with nasal
step of Roenne,
# $   

‡ Peripheral scotoma that spreads and


coalesce to the paracentral scotoma ^
‡ Leaving central island and accompanying
temporal island, even if the central vision is
still normal
‡ Temporal island ^ total blindness
# $ 
  
  

‡ Primary open-angle glaucoma


‡ Secondary open-angle glaucoma
‡ Primary closed-angle glaucoma
‡ Secondary closed-angle glaucoma
‡ Primary congenital glaucoma
‡ Secondary congenital glaucoma
r  '   
    
‡ Bilaterally, not necessarily symmetrical, absence
of secondary causes of high IOP,
‡ ulaucomatous optic nerve damage,
‡ Open and normal angle, IOP > 21 mm g,
‡ |dult onset, hereditary, steroid responsiveness,
‡ ulaucomatous visual field defects, central tunnel
vision,
‡ Minimal clinical signs.
4   r  
   
‡ Initial therapy is usually medical, except in
advanced cases,
‡ |rgon laser trabeculoplasty (|LT) if IOP is
uncontrolled despite maximal tolerated medical
therapy,
‡ Trabeculectomy with / without antimetabolic drug
in refractory glaucoma,
‡ |rtificial filtering shunt: |chmed valve, Molteno
tube, Krupin- Denver valve.
     
   
‡ Uncontrolled IOP by maximal medical
treatment
‡ Progressive disc damage and visual field
defect
‡ Drugs intolerance
‡ Unable to buy the drugs
‡ Poor compliance
‡ Unable to do the regular control
r   '   
‡ Obstruction of aqueous outflow as a result
of closure of the angle by the peripheral iris
‡ |natomically predisposed, bilateral,
‡ Predisposition:
± Crowded anterior segment
± Relatively anterior location iris lens diaphragm,
± Shallow anterior chamber,
± Narrow entrance to the chamber angle.
r 

‡ Five overlapping stage:


± Latent
± Intermittent (sub acute)
± |cute (congestive and post congestive)
± Chronic
± |bsolute
å    '   

‡ Shallow anterior chamber, convex-shape


iris lens diaphragm, close iris to cornea,
normal IOP, occludable angle,
‡ Treatment:
± uood fellow eye ^ without treatment, follow
up,
± P|Cu fellow eye ^ laser iridotomy.
    
 '   
‡ Rapid partial closure anterior chamber angle
and reopening of the angle after some rest,
‡ Precipitating factors: physiological
mydriasis, watching TV in dark room,
prone position, reading, sewing, emotion,
stress,
‡ Transient blurring of vision, halo, headache,
‡ Recovery after some rest.
   "
 '   
‡ Presentation:
± Rapidly progressive impairment of
vision, sometimes the vision 1/300 ± 0,
± Eye ache and frontal headache,
± Congestion, nausea, vomiting.
   "
 '   
‡ Examination
± Ciliary and conjunctival injection
± IOP > 50 mm g, dilated pupil,
unreactive.
± Cornea: epithelial edema, KP(+), vesicle
± |nt chamber: shallow ^ P|S, flare / cell
(+),
   "
 '   

‡ Wide pupil, slow / negative light


reflex,
‡ Papilla edema, retinal edema,
   " 
 '   
   "
 '   
‡ Differential diagnosis:
± Red eyes:
‡ acute glaucoma, conjunctivitis, iridocyclitis
± Silent eyes:
‡ simple glaucoma, ocular hypertension
± ulaucomatous visual field defect:
‡ anomaly of the optic nerve and retina
± Papillary atrophy:
‡ anomaly at optic nerve
± Congenital megalocornea without high IOP
   "
 '   
‡ Treatment:
± Immediately decrease IOP with maximal drugs,
± Wait for 24 hours ^ evaluation,
± Normal IOP, deep |C, open angle ^
iridectomy,
± igh IOP, permanent |C closure > 50% ^
trabeculectomy,
± The fellow eye: preventive iridectomy.
r   "
 '   

   '   
‡ Clinical features of chronic C|u are similar as
PO|u except gonioscopy of the angle is closed,
‡ There are three mechanism of CC|u:
± Creeping P|S ^ laser iridotomy / trabeculectomy
± |fter intermittent and laser iridotomy ^ drug >
± Combination of PO|u with narrow angle ^ laser
iridotomy + medical ^ trabeculectomy

   '   

‡ Signs and therapy are similar as simple


glaucoma:
± Trabeculectomy,
± Laser gonioplasty to make an angle,
± |rgon Laser Trabeculopasty (|LT)
r     

‡ 65% of patients are male, 1: 10.000,


‡ Inheritance is autosomal recessive, bilateral,
‡ Maldevelopment of the trabeculum and
iridotrabecular junction, abscent of angle
recess, trabeculodysgenesis,
‡ The iris insertion can be flat or concave,
‡ Poorly prognosis.
r     

‡ Clinical signs:
± Depends on the age of onset and the level of
IOP,
± |ccording to age of onset there are 3 types:
‡ True congenital glaucoma (40%). IOP elevated
intrauterine ^ buphthalmos,
‡ Infantile glaucoma (55%) manifest after birth,
‡ Juvenile glaucoma: IOP » at 2-16 years of age, with
clinical manifestation the same as PO|u.
r      
‡ Examinations:
± Corneal haze, lacrimation, photophobia and
blepharospasm,
± Buphthalmos if IOP » before the age of 3
usually associated with axial myop, subluxated
lens,
± Break of Descemet membrane, endothelial
decompensation ^ permanent stromal edema,
± Reversible glaucomatous cupping.
r     

‡ Treatment:
± Initial drug treatment,
± uoniotomy if cornea is still clear,
± Trabeculotomy at corneal clouding,
± Trabeculectomy and trabeculotomy,
± Trabeculectomy with antimetabolic agent,
± Outcome of the operation is poor.
    
‡ Inflammation and residual inflammation of
the uveal tissue: iridocyclitis, posterior
synechia,
‡ Immature cataract, hipermature cataract,
‡ Lens luxation, lens subluxation,
‡ Ischemic retina,
‡ Sub choroidal bleeding,
‡ Congenital anomaly of the eye
    

‡ Pigmentary gl. - Neovascular gl.


‡ Inflammatory gl. - Phacolytic glaucoma
‡ Red cell gl. - uhost cell glaucoma
‡ |ngle recession glaucoma
‡ Iridocorneal endothelial syndrome
‡ Pseudoexfoliative glaucoma

 
‡ Nerve fiber damage caused by glaucoma is
irreversible,
‡ Principal of therapy is to decrease IOP medically
or surgically to maintain the current condition,
‡ The purposes of decreasing the IOP is to reduce
progressivity of the nerve fiber damage and visual
field defect,
‡ Early finding.
    4    

‡ Simple glaucoma
‡ |cute / chronic closed angle glaucoma
‡ Maintain the diurnal IOP
‡ Lowering IOP before operation
X     
‡ Carbonic anhydrase inhibitor ^
± acetazolamide 250 mg qid orally,
± dorzolamide eye drop tid,
‡ Beta-adrenergic antagonist:
± beta-blocker (timolol maleat 0.25-0.5%) bid,
± betaxolol 0.25% - 0.5% bid.
‡ |drenergic agonist:
± depefeprine 0.5% - 2% bid.

   
‡ Parasympathomimetic agents:
± pilocarpin eye drop 2-4%, 2-6 x / day
± carbachol 0.75% used after cataract operation
‡ Increase the latanoprost uveoscleral flow
‡ yperosmotic fluid
± glycerol 50% 1-2 ml/kg body weight, drink all at once,
± manitol 20% swift infusion preoperative, 1.5-3 ml/kg
body weight.
   
‡ Peripheral iridectomy:
± |cute attack glaucoma, with good trabecular
meshwork,
± Preventive treatment from acute attack for the fellow
eye.
‡ Trabeculectomy for all types of glaucoma,
‡ uoniotomy for congenital glaucoma if the cornea
is still clear,
‡ Trabeculotomy for congenital glaucoma if the
cornea is edema.
   
‡ Treatment for absolute glaucoma:
± cyclocryo coagulation destroys the ciliary body
to decrease | production,
± enucleation if all treatment is not successfull.
‡ Laser treatment:
± iridotomy
± gonioplasty
± trabeculoplasty
 r  

‡ Early and right diagnosis,


‡ |dequate control of IOP by medical /
surgical treatment,
‡ Compliance of the patients for checking
their IOP and use medical treatment,
‡ Case finding among glaucoma family.
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